Evidence map›Paper›PMID 41615805›Full record

ArticleCell reports2026

PD-L1 is an intrinsic switch for natural killer cell-mediated, TRAIL-dependent antiviral function.

Kayla Frank, Himani Sharma, Efthymios Motakis, Nooshin Nourbakhsh, Shawn Abeynaike, Tridu R Huynh, Cheryl A Jones, Scott K Johnson, S Mark Tompkins, Silke Paust

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Kayla FrankDepartment of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA, USA; The Skaggs Graduate Program in Chemical and Biological Sciences, The Scripps Research Institute, La Jolla, CA, USA.
Himani SharmaThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Efthymios MotakisThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Nooshin NourbakhshThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Shawn AbeynaikeDepartment of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA, USA; The Skaggs Graduate Program in Chemical and Biological Sciences, The Scripps Research Institute, La Jolla, CA, USA.
Tridu R HuynhDepartment of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA, USA; Division of Internal Medicine, Scripps Clinic/Scripps Green Hospital, La Jolla, CA, USA.
Cheryl A JonesCenter for Vaccines and Immunology, University of Georgia, Athens, GA, USA.
Scott K JohnsonCenter for Vaccines and Immunology, University of Georgia, Athens, GA, USA.
S Mark TompkinsCenter for Vaccines and Immunology, University of Georgia, Athens, GA, USA.
Silke PaustDepartment of Immunology and Microbiology, The Scripps Research Institute, La Jolla, CA, USA; The Skaggs Graduate Program in Chemical and Biological Sciences, The Scripps Research Institute, La Jolla, CA, USA; The Jackson Laboratory for Genomic Medicine, Farmington, CT, USA. Electronic address: silke.paust@jax.org.

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Novel mechanisms regulating immunity to respiratory virus infectionR01AI174590 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI PAUST, SILKE · 2023 to 2025
$3.5M
NCI NIH HHS P30 CA034196NIAID NIH HHS R01 AI174590
6 · The paper itself

Abstract

Each year, influenza A virus (IAV) infection of the lung causes half a million deaths worldwide. Patients with compromised immunity experience distinct influenza pathogenesis; however, most IAV-related research is done with wild-type mice or people who are otherwise healthy. We utilize a model of immunocompromised recombination-activating gene 1 (Rag1)-knockout (KO) mice to discover natural killer (NK) cell activation and regulation mechanisms during IAV infection. The treatment of IAV-challenged Rag1-KO mice with a monoclonal antibody (mAb) targeting programmed death ligand 1 (PD-L1) triggers NK cell-intrinsic signaling of PD-L1 and significantly delays lethality. This treatment upregulates tumor necrosis factor-related apoptosis-inducing ligand on NK cells downstream of PD-L1 signaling and is required for the benefits of PD-L1 mAb treatment in IAV-challenged Rag1-KO mice. These results present a paradigm shift for understanding the innate immune response to respiratory virus infections, offering an alternative approach for therapeutic treatment of IAV infections in patients with compromised immunity.

Indexed as

B7-H1 AntigenKiller Cells, NaturalOrthomyxoviridae InfectionsTNF-Related Apoptosis-Inducing LigandAnimalsAntibodies, MonoclonalHomeodomain ProteinsHumansImmunity, InnateInfluenza A virusMiceMice, Inbred C57BLMice, KnockoutSignal TransductionAntibodies, MonoclonalB7-H1 AntigenCd274 protein, mouseHomeodomain ProteinsRAG-1 proteinTNF-Related Apoptosis-Inducing LigandTnfsf10 protein, mouseCP: immunologyimmunocompromisedinfluenzaNK cellsPD-L1TRAIL

Identifiers

PMID41615805
PMCPMC13101560

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.